The lungs function both to secure the transport of oxygen (O2) from inspired gas to the blood for metabolism by the cells, and that the byproduct of metabolism, carbon dioxide (CO2), is transported from the blood to the alveolar air to be expired. The function of the lungs in this process, known as pulmonary gas exchange, is vital for maintaining homeostatis, and pulmonary gas exchange disorders as seen for example in patients with chronic obstructive pulmonary disease (COPD), postoperative patients and the critically ill are major causes of death in hospitalized patients, and are associated with large socioeconomic costs in and out of hospitals.
In individuals where pulmonary gas exchange is compromised, blood levels of O2 and CO2 are affected differently by the underlying causes of gas exchange problems. The most common cause of pulmonary gas exchange problems is ventilation/perfusion ({dot over (V)}/{dot over (Q)}) mismatch, where pulmonary shunt ({dot over (V)}/{dot over (Q)}=0) and alveolar dead space ({dot over (V)}/{dot over (Q)}=infinite) represent the extremes. The transport of O2 from the lungs to the blood is most affected by pulmonary shunt and regions of the lung with low {dot over (V)}/{dot over (Q)} ratios caused by pulmonary injuries such as atelectasis and airway closure. In contrast, the transport of CO2 from the blood to the lungs is most affected by alveolar dead space and regions of the lung with high {dot over (V)}/{dot over (Q)} ratios.
Whilst O2 and CO2 are affected differently by pulmonary gas exchange disorders, transport of the two gases in the body is not independent. Both O2 and CO2 are transported in the body by blood with the mechanisms for binding the two gases in blood being different. O2 is mainly transported bound to haemoglobin, whereas CO2 is mainly transported in the form of bicarbonate (HCO3). The transport of O2 and CO2 is coupled through effects known as the Bohr-Haldane effects and correct description of transport of both these gasses requires consideration of these effects.
In clinical practice, pulmonary gas exchange problems are normally evaluated using surrogate measures which give a poor indication of the true underlying problems. O2 gas exchange problems are normally evaluated using pulse oximetry oxygen saturation measurements or oxygen partial pressure or saturation analysed from an arterial blood sample. Whilst these measures indeed may indicate whether there is a O2 gas exchange problem in the form of hypoxemia, they vary with changes in therapy not affecting the gas exchange status of the patient, such as changes in inspired oxygen fraction (FiO2), and they do not allow a discrimination between whether the underlying cause is low {dot over (V)}/{dot over (Q)} or shunt, for which treatment can differ.
A previous patent describes the Automatic Lung Parameter Estimator (hereinafter referred to as the ALPE patent, or the ALPE device/system); U.S. Pat. No. 7,008,380 B, which is hereby incorporated by reference in its entirety. The patent describes a device for evaluating pulmonary gas exchange with reference to the transport of oxygen. This device has been shown to describe pulmonary gas exchange of oxygen accurately in several patient groups successfully separating the cause of O2 gas exchange problems into that arising due to shunt and low {dot over (V)}/{dot over (Q)}.
For CO2, measurements in clinical practice include an arterial blood sample giving the partial pressure of CO2 and the pH showing whether CO2 level is abnormal and whether it has led to an acidosis/alkalosis. In addition alveolar deadspace can be estimated from capnography but this is not normally performed outside the operating theater.
Despite early physiological modeling efforts in the 1940's forming much of our current understanding of pulmonary gas exchange, O2 and CO2 have traditionally been measured and evaluated independently. However, there is a clear improvement potential in combining O2 and CO2 in measurements and analysis acquiring a synergistic effect allowing relevant interactions between O2 and CO2 to be described and exploiting all available information resulting in more accurate and physiological description of pulmonary gas exchange.
Hence, an improved device for evaluating pulmonary gas exchange would be advantageous, and in particular a more efficient and/or reliable device would be advantageous.